Background: Chronic lower limb ischemia develops earlier and more frequently in patients with type 2 diabetes mellitus. Diabetes remains the main cause of lower-extremity non-traumatic amputations. Current medical treatment, based on antiplatelet therapy and statins, has demonstrated deficient improvement of the disease. In recent years, research has shown that it is possible to improve tissue perfusion through therapeutic angiogenesis. Both in animal models and humans, it has been shown that cell therapy can induce therapeutic angiogenesis, making mesenchymal stromal cell-based therapy one of the most promising therapeutic alternatives. The aim of this study is to evaluate the feasibility, safety, and efficacy of cell therapy based on mesenchymal stromal cells derived from adipose tissue intramuscular administration to patients with type 2 diabetes mellitus with critical limb ischemia and without possibility of revascularization. Methods: A multicenter, randomized double-blind, placebo-controlled trial has been designed. Ninety eligible patients will be randomly assigned at a ratio 1:1:1 to one of the following: control group (n = 30), low-cell dose treatment group (n = 30), and high-cell dose treatment group (n = 30). Treatment will be administered in a single-dose way and patients will be followed for 12 months. Primary outcome (safety) will be evaluated by measuring the rate of adverse events within the study period. Secondary outcomes (efficacy) will be measured by assessing clinical, analytical, and imaging-test parameters. Tertiary outcome (quality of life) will be evaluated with SF-12 and VascuQol-6 scales. Discussion: Chronic lower limb ischemia has limited therapeutic options and constitutes a public health problem in both developed and underdeveloped countries. Given that the current treatment is not established in daily clinical practice, it is essential to provide evidence-based data that allow taking a step forward in its clinical development. Also, the multidisciplinary coordination exercise needed to develop this clinical trial protocol will undoubtfully be useful to conduct academic clinical trials in the field of cell therapy in the near future.

Background Major adverse cardiovascular events are the main cause of morbidity and mortality over the long term in patients undergoing carotid endarterectomy. There are few reports assessing the prognostic value of markers of inflammation in relation to the risk of cardiovascular disease after carotid endarterectomy. Here, we aimed to determine whether matrix metalloproteinases (MMP-1, MMP-2, MMP-7, MMP-9 and MMP-10), tissue inhibitor of MMPs (TIMP-1) and in vivo inflammation studied by F-18-FDG-PET/CT predict recurrent cardiovascular events in patients with carotid stenosis who underwent endarterectomy. Methods This prospective cohort study was carried out on 31 consecutive patients with symptomatic (23/31) or asymptomatic (8/31) severe (> 70%) carotid stenosis who were scheduled for carotid endarterectomy between July 2013 and March 2016. In addition, 26 healthy controls were included in the study. Plasma and serum samples were collected 2 days prior to surgery and tested for MMP-1, MMP-2, MMP-7, MMP-9, MMP-10, TIMP-1, high-density lipoprotein, low-density lipoprotein, high-sensitivity C-reactive protein and erythrocyte sedimentation rate. F-18-FDG-PET/CT focusing on several territories' vascular wall metabolism was performed on 29 of the patients because of no presurgical availability in 2 symptomatic patients. Histological and immunohistochemical studies were performed with antibodies targeting MMP-10, MMP-9, TIMP-1 and CD68. Results The patients with carotid stenosis had significantly more circulating MMP-1, MMP-7 and MMP-10 than the healthy controls. Intraplaque TIMP-1 was correlated with its plasma level (r = 0.42 P = .02) and with F-18-FDG uptake (r = 0.38 P = .05). We did not find any correlation between circulating MMPs and in vivo carotid plaque metabolism assessed by F-18-FDG-PET. After a median follow-up of 1077 days, 4 cerebrovascular, 7 cardiovascular and 11 peripheral vascular events requiring hospitalization were registered. Circulating MMP-7 was capable of predicting events over and above the traditional risk factors (HR = 1.15 P = .006). When the model was associated with the variables of interest, the risk predicted by F-18-FDG-PET was not significant. Conclusions Circulating MMP-7 may represent a novel marker for recurrent cardiovascular events in patients with moderate to severe carotid stenosis. MMP-7 may reflect the atherosclerotic burden but not plaque inflammation in this specific vascular territory.

Aneurysms of the portal vein and its branches have been rarely described. Their natural history is unknown although large ones (>3 cm in diameter) have been reported to cause rupture, thrombosis, duodenal or biliary obstruction, inferior vena cava compression and/or portal hypertension. We report the case of an incidentally diagnosed 4.5 cm splenic vein aneurysm repaired by endovascular treatment through a transhepatic route. The aneurysm was successfully excluded using a covered stent (Viabahn, Gore). The transhepatic route opens the possibility of offering a minimally invasive approach to vascular lesions of the portal vein system.

Introduction In 1934 von Rosen first described a posttraumatic thrombosis of the distal ulnar artery resulting from blunt a trauma to the hypothenar region. But it was Conn in 1970 who named it the hypothenar hammer syndrome (HHS) 1-2 .

In the last 20 years, endovascular procedures have radically altered the treatment of diseases of the aorta. The objective of endovascular treatment of dissections is to close the entry point to redirect blood flow toward the true lumen, thereby achieving thrombosis of the false lumen. In extensive chronic dissections that have evolved with the formation of a large aneurysm, the dissection is maintained from the end of the endoprosthesis due to multiple orifices, or reentries, that communicate with the lumens. In addition, one of the primary limitations of this technique is when the visceral arteries have disease involvement. In this report we present a case where, despite having treated the entire length of the descending thoracic aorta, the dissection was maintained distally, leading to progression of the diameter of the aneurysm. After reviewing the literature, and to the best of our knowledge, we describe the first case in which renal autotransplant was performed to allow for subsequent exclusion of the aorta at the thoracoabdominal level using a fenestrated endoprosthesis for the celiac trunk and the superior mesenteric artery.

In the last 20 years, endovascular procedures have radically altered the treatment of diseases of the aorta. The objective of endovascular treatment of dissections is to close the entry point to redirect blood flow toward the true lumen, thereby achieving thrombosis of the false lumen. In extensive chronic dissections that have evolved with the formation of a large aneurysm, the dissection is maintained from the end of the endoprosthesis due to multiple orifices, or reentries, that communicate with the lumens. In addition, one of the primary limitations of this technique is when the visceral arteries have disease involvement. In this report we present a case where, despite having treated the entire length of the descending thoracic aorta, the dissection was maintained distally, leading to progression of the diameter of the aneurysm. After reviewing the literature, and to the best of our knowledge, we describe the first case in which renal autotransplant was performed to allow for subsequent exclusion of the aorta at the thoracoabdominal level using a fenestrated endoprosthesis for the celiac trunk and the superior mesenteric artery.

Arterial prosthetic graft infection is one of the most challenging issues in vascular surgery. We report a case of an infected descending thoracic aorta endograft, presenting itself several years after placement, with hemoptysis and back pain as referred symptoms. The patient was successfully treated by removing the thoracic aorta and replacing the infected endografts with a cryopreserved aortic allograft, running from the left subclavian artery to the aortic diaphragmatic hiatus.